Nucleic acids are released from dead and dying cells. These extracellular nucleic acids (RNAs and DNAs) can be taken up by immune cells that release inflammatory signals and can activate multiple Pattern Recognition Receptors (PRR) such as the Toll-Like Receptors (TLRs 3, 7, 8 and 9 in particular), which are localized in endosomes (Kawai and Akira, Nat. Immunol. 11(5):373-84 (2010)). The inappropriate activation of these TLRs can elicit a variety of inflammatory and autoimmune diseases, for example, systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, diabetes and chronic wounds.
It has been previously reported that certain nucleic acid-binding molecules (e.g., PAMAM-G3, CDP, HDMBr, protamine, polyethylenimine) can inhibit activation of nucleic acid-sensing PRRs, irrespective of whether they recognize ssRNA, dsRNA or hypomethylated DNA (Lee et al, Proc. Natl. Acad, Sci. USA 108(34):14055-60 (2011)). Means of using these nucleic acid binding molecules to inhibit aberrant inflammation without compromising immune responsiveness systemically are needed in the art.
In addition, biofilms often form in wound sites causing persistent inflammation and infection. These biofilms reduce the ability of the wound to heal. Means of reducing the ability of microorganisms to form biofilms are also needed. Methods of inhibiting the ability of microorganisms to grow in wound sites or in or on medical devices are also needed.